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Purpose The DBA/2J mouse has been described as a model for congenital experimental glaucoma. It develops anterior segment anomalies with synechiae and pigment dispersion leading to raised intraocular pressure (IOP) and glaucomatous damage. However there are serious practical considerations when using this model in longitudinal studies. Methods We followed 118 mice from 12 - 48 weeks of age in a pharmaceutical trial. Here we report on the findings in control animals (n=37). IOP was measured weekly, electrophysiology and optical coherence tomography (OCT) every 6 weeks. A subset also had invasive IOP measurements performed prior to euthanasia. Results While IOP eventually rose by 9 months in most animals, tonometry was complicated by corneal calcification in the majority of animals rendering IOP measurement unreliable. Invasive IOP did not correlate with non-invasive measures. Loss of scotopic threshold response and thinning of inner retinal layers on OCT was observed over time, suggesting glaucomatous damage but this occurred in some animals without raised IOP. Poor pupil dilation significantly affected electrophysiology, OCT and fundus imaging. 22% of animals developed major systemic complications leading to high dropout rate. Conclusions The DBA/2J experimental glaucoma model shows variability in expression and its pathological changes cause major difficulties in assessing disease progression. From our experience the model presents significant challenges for drug studies in glaucoma, as there are many confounding factors; difficulty with accurate IOP measurement, in vivo imaging, and electrophysiology recording and a high drop-out rate. In addition there may be an underlying neurodegenerative process independent of IOP.